Diverticula are out-pouchings of our intestine. Doctors like using a tire analogy: high pressures within the gut can force the intestines to balloon out through weak spots in the intestinal wall like an inner tube poking out through a worn tire tread. You can see what they actually look like in my video, Diverticulosis: When Our Most Common Gut Disorder Hardly Existed. These pockets can become inflamed and infected, and, to carry the tire analogy further, can blow out and spill fecal matter into the abdomen, and lead to death. Symptoms can range from no symptoms at all, to a little cramping and bloating, to "incapacitating pain that is a medical emergency." Nine out of ten people who die from the disease never even knew they had it.

The good news is there may be a way to prevent the disease. Diverticular disease is the most common intestinal disorder, affecting up to 70% of people by age 60. If it's that common, though, is it just an inevitable consequence of aging? No, it's a new disease. In 1907, 25 cases had been reported in the medical literature. Not cases in 25% of people, but 25 cases period. And diverticular disease is kind of hard to miss on autopsy. A hundred years ago, in 1916, it didn't even merit mention in medical and surgical textbooks. The mystery wasn't solved until 1971.

How did a disease that was almost unknown become the most common affliction of the colon in the Western world within one lifespan? Surgeons Painter and Burkitt suggested diverticulosis was a deficiency disease--i.e., a disease caused by a deficiency of fiber. In the late 1800s, roller milling was introduced, further removing fiber from grain, and we started to fill up on other fiber-deficient foods like meat and sugar. A few decades of this and diverticulosis was rampant.

This is what Painter and Burkitt thought was going on: Just as it would be easy to squeeze a lump of butter through a bicycle tube, it's easy to move large, soft, and moist intestinal contents through the gut. In contrast, try squeezing through a lump of tar. When we eat fiber-deficient diets, our feces can become small and firm, and our intestines have to really squeeze down hard to move them along. This buildup of pressure may force out those bulges. Eventually, a low-fiber diet can sometimes lead to the colon literally rupturing itself.

If this theory is true, then populations eating high­-fiber diets would have low rates of diverticulosis. That's exactly what's been found. More than 50% of African Americans in their 50s were found to have diverticulosis, compared to less than 1% in African Africans eating traditional plant-based diets. By less than 1%, we're talking zero out of a series of 2,000 autopsies in South Africa and two out of 4,000 in Uganda. That's about one thousand times lower prevalence.

Diverticula are out-pouchings of our intestine. Doctors like using a tire analogy: high pressures within the gut can force the intestines to balloon out through weak spots in the intestinal wall like an inner tube poking out through a worn tire tread. You can see what they actually look like in my video, Diverticulosis: When Our Most Common Gut Disorder Hardly Existed. These pockets can become inflamed and infected, and, to carry the tire analogy further, can blow out and spill fecal matter into the abdomen, and lead to death. Symptoms can range from no symptoms at all, to a little cramping and bloating, to "incapacitating pain that is a medical emergency." Nine out of ten people who die from the disease never even knew they had it.

The good news is there may be a way to prevent the disease. Diverticular disease is the most common intestinal disorder, affecting up to 70% of people by age 60. If it's that common, though, is it just an inevitable consequence of aging? No, it's a new disease. In 1907, 25 cases had been reported in the medical literature. Not cases in 25% of people, but 25 cases period. And diverticular disease is kind of hard to miss on autopsy. A hundred years ago, in 1916, it didn't even merit mention in medical and surgical textbooks. The mystery wasn't solved until 1971.

How did a disease that was almost unknown become the most common affliction of the colon in the Western world within one lifespan? Surgeons Painter and Burkitt suggested diverticulosis was a deficiency disease--i.e., a disease caused by a deficiency of fiber. In the late 1800s, roller milling was introduced, further removing fiber from grain, and we started to fill up on other fiber-deficient foods like meat and sugar. A few decades of this and diverticulosis was rampant.

This is what Painter and Burkitt thought was going on: Just as it would be easy to squeeze a lump of butter through a bicycle tube, it's easy to move large, soft, and moist intestinal contents through the gut. In contrast, try squeezing through a lump of tar. When we eat fiber-deficient diets, our feces can become small and firm, and our intestines have to really squeeze down hard to move them along. This buildup of pressure may force out those bulges. Eventually, a low-fiber diet can sometimes lead to the colon literally rupturing itself.

If this theory is true, then populations eating high­-fiber diets would have low rates of diverticulosis. That's exactly what's been found. More than 50% of African Americans in their 50s were found to have diverticulosis, compared to less than 1% in African Africans eating traditional plant-based diets. By less than 1%, we're talking zero out of a series of 2,000 autopsies in South Africa and two out of 4,000 in Uganda. That's about one thousand times lower prevalence.

What has driven the dramatic increase in prevalence of the inflammatory bowel disease Crohn's disease in societies that rapidly westernized--a disease practically unknown just a century ago? What has changed in our internal and external environment that has led to the appearance of this horrible disease?

Japan suffered one of the most dramatic increases, and out of all the changing dietary components, animal protein appeared to be the strongest factor. There was an exponential increase in newly diagnosed Crohn's patients and daily animal protein intake, whereas the greater the vegetable protein, the fewer the cases of Crohn's, which is consistent with data showing a more plant-based diet may be successful in both preventing and treating Crohn's disease (See Preventing Crohn's Disease With Dietand Dietary Treatment of Crohn's Disease). But what about other inflammatory bowel diseases?

In the largest study of its kind, shown in my video Preventing Ulcerative Colitis with Diet, 60,000 people were followed for more than a decade. Researchers found that high total protein intake--specifically animal protein--was associated with a significantly increased risk of the other big inflammatory bowel disease, ulcerative colitis. It wasn't just protein in general, but the "association between high protein intake and inflammatory bowel disease risk was restricted to animal protein."Since World War II, animal protein intake has increased not only in Japan but also in all developed countries. This increase in animal protein consumption is thought to explain some of the increased incidence of inflammatory bowel disease in the second half of the 20th century.

Other studies found this as well, but why? What's the difference between animal protein and plant protein? Animal proteins tend to have more sulfur containing amino acids like methionine, which bacteria in our gut can turn into the toxic rotten egg smell gas, hydrogen sulfide. Emerging evidence suggests that sulfur compounds may play a role in the development of ulcerative colitis, a chronic inflammatory disease of the colon and rectum characterized by bloody diarrhea.

The first hint as to the importance of our gut flora was in the 1970's when "analysis of stools showed that their bulk was made up of mostly bacteria, not undigested material." We're pushing out trillions of bacteria a day and they just keep multiplying and multiplying. They do wonderful things for us like create the protective compound, butyrate, from the fiber we eat, but unfortunately, the bacteria may also elaborate toxic products from food residues such as hydrogen sulfide "in response to a high-meat diet."

Hydrogen sulfide is a bacterially derived cell poison that has been implicated in ulcerative colitis. We had always assumed that sulfide generation in the colon is driven by dietary components such as sulfur-containing amino acids, but we didn't know for sure until a study from Cambridge was published. Researchers had folks eat five different diets each with escalating meat contents from vegetarian all the way up to a steak each day. They found that the more meat one ate, the more sulfide; ten times more meat meant ten times more sulfide. They concluded that "dietary protein from meat is an important substrate for sulfide generation by bacteria in the human large intestine."

Hydrogen sulfide can then act as a free radical and damage our DNA at concentrations way below what our poor colon lining is exposed to on a routine basis, which may help explain why diets higher in meat and lower in fiber may produce so-called "fecal water" that causes about twice as much DNA damage. Fecal water is like when researchers make a tea from someone's stool.

The biology of sulfur in the human gut has escaped serious attention until recently. Previously it was just thought of as the rotten egg smell in malodorous gas, but the increase in sulfur compounds in response to a supplement of animal protein is not only of interest in the field of flatology--that is, the formal study of farts--but may also be of importance in the development of ulcerative colitis.

What has driven the dramatic increase in prevalence of the inflammatory bowel disease Crohn's disease in societies that rapidly westernized--a disease practically unknown just a century ago? What has changed in our internal and external environment that has led to the appearance of this horrible disease?

Japan suffered one of the most dramatic increases, and out of all the changing dietary components, animal protein appeared to be the strongest factor. There was an exponential increase in newly diagnosed Crohn's patients and daily animal protein intake, whereas the greater the vegetable protein, the fewer the cases of Crohn's, which is consistent with data showing a more plant-based diet may be successful in both preventing and treating Crohn's disease (See Preventing Crohn's Disease With Dietand Dietary Treatment of Crohn's Disease). But what about other inflammatory bowel diseases?

In the largest study of its kind, shown in my video Preventing Ulcerative Colitis with Diet, 60,000 people were followed for more than a decade. Researchers found that high total protein intake--specifically animal protein--was associated with a significantly increased risk of the other big inflammatory bowel disease, ulcerative colitis. It wasn't just protein in general, but the "association between high protein intake and inflammatory bowel disease risk was restricted to animal protein."Since World War II, animal protein intake has increased not only in Japan but also in all developed countries. This increase in animal protein consumption is thought to explain some of the increased incidence of inflammatory bowel disease in the second half of the 20th century.

Other studies found this as well, but why? What's the difference between animal protein and plant protein? Animal proteins tend to have more sulfur containing amino acids like methionine, which bacteria in our gut can turn into the toxic rotten egg smell gas, hydrogen sulfide. Emerging evidence suggests that sulfur compounds may play a role in the development of ulcerative colitis, a chronic inflammatory disease of the colon and rectum characterized by bloody diarrhea.

The first hint as to the importance of our gut flora was in the 1970's when "analysis of stools showed that their bulk was made up of mostly bacteria, not undigested material." We're pushing out trillions of bacteria a day and they just keep multiplying and multiplying. They do wonderful things for us like create the protective compound, butyrate, from the fiber we eat, but unfortunately, the bacteria may also elaborate toxic products from food residues such as hydrogen sulfide "in response to a high-meat diet."

Hydrogen sulfide is a bacterially derived cell poison that has been implicated in ulcerative colitis. We had always assumed that sulfide generation in the colon is driven by dietary components such as sulfur-containing amino acids, but we didn't know for sure until a study from Cambridge was published. Researchers had folks eat five different diets each with escalating meat contents from vegetarian all the way up to a steak each day. They found that the more meat one ate, the more sulfide; ten times more meat meant ten times more sulfide. They concluded that "dietary protein from meat is an important substrate for sulfide generation by bacteria in the human large intestine."

Hydrogen sulfide can then act as a free radical and damage our DNA at concentrations way below what our poor colon lining is exposed to on a routine basis, which may help explain why diets higher in meat and lower in fiber may produce so-called "fecal water" that causes about twice as much DNA damage. Fecal water is like when researchers make a tea from someone's stool.

The biology of sulfur in the human gut has escaped serious attention until recently. Previously it was just thought of as the rotten egg smell in malodorous gas, but the increase in sulfur compounds in response to a supplement of animal protein is not only of interest in the field of flatology--that is, the formal study of farts--but may also be of importance in the development of ulcerative colitis.

If the fructose in sugar and high fructose corn syrup has been considered "alcohol without the buzz" in terms of the potential to inflict liver damage, what about the source of natural fructose, fruit?

If you compare the effects of a diet restricting fructose from both added sugars and fruit to one just restricting fructose from added sugars, the diet that kept the fruit did better. People lost more weight with the extra fruit present than if all fructose was restricted. Only industrial, not fruit fructose intake, was associated with declining liver function and high blood pressure. Fructose from added sugars was associated with hypertension; fructose from natural fruits is not.

If we have people drink a glass of water with three tablespoons of table sugar in it, which is like a can of soda, they get a big spike in blood sugar within the first hour (as you can see in my video If Fructose is Bad, What About Fruit?). Our body freaks out and releases so much insulin we actually overshoot, and by the second hour we're relatively hypoglycemic, dropping our blood sugar below where they were when we started out fasting. In response, our body dumps fat into our blood stream as if we're starving, because our blood sugars just dropped so low so suddenly.

What if you eat blended berries in addition to the sugar? They have sugars of their own in them, in fact an additional tablespoon of sugar worth, so the blood sugar spike should be worse, right?

Not only is there no additional blood sugar spike, there was no hypoglycemic dip afterwards. Blood sugar just went up and down without that overshoot and without the surge of fat into the blood.

This difference may be attributed to the semisolid consistency of the berry meals, which may have decreased the rate of stomach emptying compared with just guzzling sugar water. In addition, the soluble fiber in the berries has a gelling effect in our intestines that slows the release of sugars. To test to see if it was the fiber, researchers repeated the experiment with berry juice that had all the sugar but none of the fiber. A clear difference was observed early on in the blood sugar insulin responses. At the 15-minute mark, the blood sugar spike was significantly reduced by the berry meals, but not by the juices, but the rest of the beneficial responses were almost the same between the juice and the whole fruit, suggesting that fiber may just be part of it. It turns out there are fruit phytonutrients that inhibit the transportation of sugars through the intestinal wall into our blood stream. Phytonutrients in foods like apples and strawberries can block some of the uptake of sugars by the cells lining our intestines.

Adding berries can actually blunt the insulin spike from high glycemic foods. For example, white bread creates a big insulin spike within two hours after eating it. Eat that same white bread with some berries, though, and we're able to blunt the spike. So, even though we've effectively added more sugars in the form of berries, there's less of an insulin spike, which has a variety of potential short and long-term benefits. So if you're going to make pancakes, make sure they're blueberry pancakes.